scholarly journals Investigation of the Possible Role of RAD9 in Post-Diapaused Embryonic Development of the Brine Shrimp Artemia sinica

Genes ◽  
2019 ◽  
Vol 10 (10) ◽  
pp. 768
Author(s):  
Huifang Huang ◽  
Ce Chen ◽  
Feng Yao ◽  
Xiuling Li ◽  
Yanan Wang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Embryonic Development ◽  
Expression Pattern ◽  
Brine Shrimp ◽  
Immunofluorescence Assay ◽  
Cell Cycle Checkpoint ◽  
Organ Specificity ◽  
Related Factor ◽  
Gene Encoding ◽  
Artemia Sinica

Background: The cell cycle checkpoint protein RAD9 is a vital cell cycle regulator in eukaryotic cells. RAD9 is involved in diverse cellular functions by oligomer or monomer. However, the specific mechanism of its activity remains unknown in crustaceans, especially in embryonic diapause resumption of the brine shrimp Artemia sinica. Methods and Results: In the present article, a 1238 bp full-length cDNA of As–RAD9 gene, encoding 376 amino acids, was obtained from A. sinica. The expression pattern of As–RAD9 was analyzed by qPCR and Western blot. The mRNA expression level climbs to the top at the 10 h stage of embryo development, while the protein expression pattern is generally consistent with qPCR results. Moreover, the As–RADd9 related signaling proteins, As–RAD1, As–HUS1, As–RAD17, and As–CHK1, were also detected. Immunofluorescence assay showed that the location of As–RAD9 did not show tissue or organ specificity, and the intracellular expression was concentrated in the cytoplasm more than in the nucleus. We also explored the amount of As–RAD9 under the stresses of cold and high salinity, and the results indicate that As–RAD9 is a stress-related factor, though the mechanisms may be different in response to different stresses. Knocking down of the As–RAD9 gene led to embryonic development delay in A. sinica. Conclusions: All these results reveal that As–RAD9 is necessary for post-diapaused embryonic development in A. sinica.

Cloning and the expression pattern of Spätzle gene during embryonic development and bacterial challenge in Artemia sinica

2011 ◽  
Vol 39 (5) ◽  
pp. 6035-6042 ◽  
Author(s):  
Lu-ping Zheng ◽  
Lin Hou ◽  
Miao Yu ◽  
Xiang Li ◽  
Xiang-yang Zou
Keyword(s):  
Embryonic Development ◽  
Expression Pattern ◽  
Bacterial Challenge ◽  
Artemia Sinica

scholarly journals The Aspergillus nidulans snt Genes Are Required for the Regulation of Septum Formation and Cell Cycle Checkpoints

Genetics ◽  
2001 ◽  
Vol 159 (2) ◽  
pp. 557-569
Author(s):  
Peter R Kraus ◽  
Steven D Harris
Keyword(s):  
Cell Cycle ◽  
Aspergillus Nidulans ◽  
Nuclear Division ◽  
Threshold Level ◽  
Cell Cycle Checkpoint ◽  
Cell Cycle Checkpoints ◽  
Gene Encoding ◽  
Temporal Regulation ◽  
Septum Formation ◽  
Cycle Checkpoint

Abstract In Aspergillus nidulans, germinating conidia undergo multiple rounds of nuclear division before forming a septum. Previous genetic results suggest that the ability to separate nuclear division and septum formation depends upon a threshold level of activity of the cyclin-dependent kinase NIMXcdk1. Mutations in nimX and nimT, the gene encoding the NIMXcdk1-activating phosphatase, have revealed that Tyr-15 phosphorylation is important for determining the timing of the formation of the first septum. Here, we describe a screen for suppressors of nimT23 (snt), designed to identify additional components of the pathway regulating septum formation. We show that a subset of the snt mutants are defective in the temporal regulation of septum formation and in cell cycle checkpoint responses. Molecular characterization of sntA shows that it is allelic to the previously described ankA gene, which encodes the NIMXcdk1 Tyr-15 kinase. Additional experiments described in this study show that nutritional conditions modulate the timing of septum formation and alter the phenotypes displayed by the snt mutants. A model that suggests that the timing of septum formation is influenced by DNA damage and glucose availability via the sntA and sntB gene products is proposed.

Cell Cycle Checkpoint Genes and Aneuploidy: A Short Review

2001 ◽  
Vol 2 (2) ◽  
pp. 171-180 ◽  
Author(s):  
William Kearns ◽  
Johnson Liu
Keyword(s):  
Cell Cycle ◽  
Short Review ◽  
Cell Cycle Checkpoint ◽  
Cycle Checkpoint ◽  
Checkpoint Genes

scholarly journals Acceleration or Brakes: Which Is Rational for Cell Cycle-Targeting Neuroblastoma Therapy?

Biomolecules ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 750
Author(s):  
Kiyohiro Ando ◽  
Akira Nakagawara
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Progression ◽  
Parp Inhibitors ◽  
Cell Cycle Checkpoint ◽  
Mitotic Catastrophe ◽  
Malignant Neoplasms ◽  
Checkpoint Kinases ◽  
Molecular Features ◽  
Cycle Checkpoint

Unrestrained proliferation is a common feature of malignant neoplasms. Targeting the cell cycle is a therapeutic strategy to prevent unlimited cell division. Recently developed rationales for these selective inhibitors can be subdivided into two categories with antithetical functionality. One applies a “brake” to the cell cycle to halt cell proliferation, such as with inhibitors of cell cycle kinases. The other “accelerates” the cell cycle to initiate replication/mitotic catastrophe, such as with inhibitors of cell cycle checkpoint kinases. The fate of cell cycle progression or arrest is tightly regulated by the presence of tolerable or excessive DNA damage, respectively. This suggests that there is compatibility between inhibitors of DNA repair kinases, such as PARP inhibitors, and inhibitors of cell cycle checkpoint kinases. In the present review, we explore alterations to the cell cycle that are concomitant with altered DNA damage repair machinery in unfavorable neuroblastomas, with respect to their unique genomic and molecular features. We highlight the vulnerabilities of these alterations that are attributable to the features of each. Based on the assessment, we offer possible therapeutic approaches for personalized medicine, which are seemingly antithetical, but both are promising strategies for targeting the altered cell cycle in unfavorable neuroblastomas.

scholarly journals Inhibition of Aurora Kinase B activity disrupts development and differentiation of salivary glands

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Abeer K. Shaalan ◽  
Tathyane H. N. Teshima ◽  
Abigail S. Tucker ◽  
Gordon B. Proctor
Keyword(s):  
Cell Cycle ◽  
Embryonic Development ◽  
Salivary Glands ◽  
Aurora Kinase ◽  
Serine Threonine Kinase ◽  
Aurora Kinase B ◽  
Development And Differentiation ◽  
Differentiation Marker ◽  
Key Events

AbstractLittle is known about the key molecules that regulate cell division during organogenesis. Here we determine the role of the cell cycle promoter aurora kinase B (AURKB) during development, using embryonic salivary glands (E-SGs) as a model. AURKB is a serine/threonine kinase that regulates key events in mitosis, which makes it an attractive target for tailored anticancer therapy. Many reports have elaborated on the role of AURKB in neoplasia and cancer; however, no previous study has shown its role during organ development. Our previous experiments have highlighted the essential requirement for AURKB during adult exocrine regeneration. To investigate if AURKB is similarly required for progression during embryonic development, we pharmacologically inhibited AURKB in developing submandibular glands (SMGs) at embryonic day (E)13.5 and E16.5, using the highly potent and selective drug Barasertib. Inhibition of AURKB interfered with the expansion of the embryonic buds. Interestingly, this effect on SMG development was also seen when the mature explants (E16.5) were incubated for 24 h with another cell cycle inhibitor Aphidicolin. Barasertib prompted apoptosis, DNA damage and senescence, the markers of which (cleaved caspase 3, γH2AX, SA-βgal and p21, respectively), were predominantly seen in the developing buds. In addition to a reduction in cell cycling and proliferation of the epithelial cells in response to AURKB inhibition, Barasertib treatment led to an excessive generation of reactive oxygen species (ROS) that resulted in downregulation of the acinar differentiation marker Mist1. Importantly, inhibition of ROS was able to rescue this loss of identity, with Mist1 expression maintained despite loss of AURKB. Together, these data identify AURKB as a key molecule in supporting embryonic development and differentiation, while inhibiting senescence-inducing signals during organogenesis.

scholarly journals Pt(II)-Thiocarbohydrazone Complex as Cytotoxic Agent and Apoptosis Inducer in Caov-3 and HT-29 Cells through the P53 and Caspase-8 Pathways

2021 ◽  
Vol 14 (6) ◽  
pp. 509
Author(s):  
Abeer A. Ibrahim ◽  
Mohanad M. Kareem ◽  
Taghreed H. Al-Noor ◽  
Tahani Al-Muhimeed ◽  
Abeer A. AlObaid ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Immunofluorescence Assay ◽  
Cell Cycle Distribution ◽  
Caspase 8 ◽  
Ovarian Adenocarcinoma ◽  
Fragmentation Test ◽  
Cycle Arrest ◽  
Apoptosis Inducer ◽  
Test Flow ◽  
Ht 29

In this study, a platinum(II) complex ([Pt(H2L)(PPh3)] complex) containing a thiocarbohydrazone as the ligand was tested as an anti-proliferative agent against ovarian adenocarcinoma (Caov-3) and human colorectal adenocarcinoma (HT-29) through MTT assays. Apoptotic markers were tested by the AO/PI double staining assay and DNA fragmentation test. Flow cytometry was conducted to measure cell cycle distribution, while the p53 and caspase-8 pathways were tested via immunofluorescence assay. Results demonstrated that the cytotoxic effect of the Pt(II)-thiocarbohydrazone complexes against Caov-3 and HT-29 cells was highly significant, and this effect triggered the activation of the p53 and caspase-8 pathways. Besides, apoptosis stimulated by the Pt(II)-thiocarbohydrazone complex was associated with cell cycle arrest at the G0/G1 phase. These findings suggest that the target complex inhibited the proliferation of Caov-3 and HT-29 cells, resulting in the arrest of the cell cycle and induction of apoptosis via the stimulation of the p53 and caspase-8 pathways. The present data suggests that the Pt(II)-thiocarbohydrazone complex could also be a promising chemotherapeutic agent for other types of cancer cells.

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